ArticleDisease models & mechanisms2015
Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 69 citations in OpenAlex.
- Pirfenidone treatment attenuates fibrosis in autosomal dominant polycystic kidney disease.JCI insight · 2026Article
- Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease.Cell communication and signaling : CCS · 2026Article
- Taohong Siwu Decoction relieves renal fibrosis: based on network pharmacology and experimental confirmation.Renal failure · 2025Article
- Fidaxomicin Reduces Collagen Expression in Intestinal Fibroblasts Via Platelet-Derived Growth Factor Receptor Beta and Glycogen Synthase Kinase-3 Beta Inhibition.Gastroenterology · 2025Article
- Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).International journal of molecular medicine · 2025Review
- Aloe-emodin ameliorates chronic kidney disease fibrosis by inhibiting PI3K-mediated signaling pathway.European journal of histochemistry : EJH · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Hypothermia Mitigates Renal Fibrosis Through the Upregulation of PGC-1α After Ischemia-Reperfusion Injury.Biomedicines · 2025Article
- Circadian Clock Disruption and Growth of Kidney Cysts in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Modulation of TGF-β signaling new approaches toward kidney disease and fibrosis therapy.International journal of biological sciences · 2025Review
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.Biogerontology · 2024Review
- Mechanistic Implications of GSK and CREB Crosstalk in Ischemia Injury.Neurotoxicity research · 2023Review
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- Long non-coding RNA FABP5P3/miR-22 axis improves TGFβ1-induced fatty acid oxidation deregulation and fibrotic changes in proximal tubular epithelial cells of renal fibrosis.Cell cycle (Georgetown, Tex.) · 2023Article
- Renalase Prevents Renal Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Down-Regulating GSK-3β/Snail Signaling.International journal of medical sciences · 2023Article
- Myofibroblast depletion reduces kidney cyst growth and fibrosis in autosomal dominant polycystic kidney disease.Kidney international · 2023Article
- Vasopressin Receptor Type-2 Mediated Signaling in Renal Cell Carcinoma Stimulates Stromal Fibroblast Activation.International journal of molecular sciences · 2022Article
- Chinese herbal decoction astragalus and angelica exerts its therapeutic effect on renal interstitial fibrosis through the inhibition of MAPK, PI3K-Akt and TNF signaling pathways.Genes & diseases · 2022Article
- The Effect of CHIR 99021, a Glycogen Synthase Kinase-3β Inhibitor, on Transforming Growth Factor β-Induced Tenon Fibrosis.Investigative ophthalmology & visual science · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Glycogen synthase kinase-3β (GSK3β) is a serine/threonine protein kinase that plays an important role in renal tubular injury and regeneration in acute kidney injury. However, its role in the development of renal fibrosis, often a long-term consequence of acute kidney injury, is unknown. Using a mouse model of renal fibrosis induced by ischemia-reperfusion injury, we demonstrate increased GSK3β expression and activity in fibrotic kidneys, and its presence in myofibroblasts in addition to tubular epithelial cells. Pharmacological inhibition of GSK3 using TDZD-8 starting before or after ischemia-reperfusion significantly suppressed renal fibrosis by reducing the myofibroblast population, collagen-1 and fibronectin deposition, inflammatory cytokines, and macrophage infiltration. GSK3 inhibition in vivo reduced TGF-β1, SMAD3 activation and plasminogen activator inhibitor-1 levels. Consistently in vitro, TGF-β1 treatment increased GSK3β expression and GSK3 inhibition abolished TGF-β1-induced SMAD3 activation and α-smooth muscle actin (α-SMA) expression in cultured renal fibroblasts. Importantly, overexpression of constitutively active GSK3β stimulated α-SMA expression even in the absence of TGF-β1 treatment. These results suggest that TGF-β regulates GSK3β, which in turn is important for TGF-β-SMAD3 signaling and fibroblast-to-myofibroblast differentiation. Overall, these studies demonstrate that GSK3 could promote renal fibrosis by activation of TGF-β signaling and the use of GSK3 inhibitors might represent a novel therapeutic approach for progressive renal fibrosis that develops as a consequence of acute kidney injury.
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